Pingueculae may enlarge slowly over time, but are a benign condition, usually requiring no treatment. Artificial tears may help to relieve discomfort, if it occurs. If cosmesis is a concern, surgical excision is sometimes done. Occasionally, a pinguecula may become inflamed, a condition called pingueculitis. The cause of pingueculitis is unknown and there are no known infectious agents associated with it. If an inflamed pinguecula is causing discomfort or cosmetic concerns, it may be treated with an anti-inflammatory agent, such as prednisolone drops.

In very severe cases of necrotizing scleritis, eye surgery must be performed to repair damaged corneal tissue in the eye and preserve the patient's vision. For less severe cases, nonsteroidal anti-inflammatory drugs, such as ibuprofen, are prescribed for pain relief. Scleritis itself is treated with an oral medication containing corticosteroids and an eye solution. In some cases, antibiotics are prescribed. Simply using eye drops will not treat scleritis. In more aggressive cases of scleritis, chemotherapy (such as systemic immunosuppressive therapy with such drugs as cyclophosphamide or azathioprine) may be used to treat the disease. If not treated, scleritis can cause blindness.

Cryotherapy (freezing) or laser photocoagulation are occasionally used alone to wall off a small area of retinal detachment so that the detachment does not spread.

Intraocular pressure can be lowered with medication, usually eye drops. Several classes of medications are used to treat glaucoma, with several medications in each class.

Each of these medicines may have local and systemic side effects. Adherence to medication protocol can be confusing and expensive; if side effects occur, the patient must be willing either to tolerate them or to communicate with the treating physician to improve the drug regimen. Initially, glaucoma drops may reasonably be started in either one or in both eyes. Wiping the eye with an absorbent pad after the administration of eye drops may result in fewer adverse effects, like the growth of eyelashes and hyperpigmentation in the eyelid.

Poor compliance with medications and follow-up visits is a major reason for vision loss in glaucoma patients. A 2003 study of patients in an HMO found half failed to fill their prescriptions the first time, and one-fourth failed to refill their prescriptions a second time. Patient education and communication must be ongoing to sustain successful treatment plans for this lifelong disease with no early symptoms.

The possible neuroprotective effects of various topical and systemic medications are also being investigated.

- Prostaglandin analogs, such as latanoprost, bimatoprost and travoprost, increase uveoscleral outflow of aqueous humor. Bimatoprost also increases trabecular outflow.

- Topical beta-adrenergic receptor antagonists, such as timolol, levobunolol, and betaxolol, decrease aqueous humor production by the epithelium of the ciliary body.

- Alpha2-adrenergic agonists, such as brimonidine and apraclonidine, work by a dual mechanism, decreasing aqueous humor production and increasing uveoscleral outflow.

- Less-selective alpha agonists, such as epinephrine, decrease aqueous humor production through vasoconstriction of ciliary body blood vessels, useful only in open-angle glaucoma. Epinephrine's mydriatic effect, however, renders it unsuitable for closed-angle glaucoma due to further narrowing of the uveoscleral outflow (i.e. further closure of trabecular meshwork, which is responsible for absorption of aqueous humor).

- Miotic agents (parasympathomimetics), such as pilocarpine, work by contraction of the ciliary muscle, opening the trabecular meshwork and allowing increased outflow of the aqueous humour. Echothiophate, an acetylcholinesterase inhibitor, is used in chronic glaucoma.

- Carbonic anhydrase inhibitors, such as dorzolamide, brinzolamide, and acetazolamide, lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body.

Often, treatment is not necessary, because episcleritis is a self-limiting condition. Artificial tears may be used to help with irritation and discomfort. More severe cases can be treated with either topical corticosteroids or oral non-steroidal anti-inflammatory drugs.

Ketorolac, a topical NSAID, may be used, but it is not more effective than artificial tears and it causes more side effects.

Because SO is so rarely encountered following eye injury, even when the injured eye is retained, the first choice of treatment may not be enucleation or evisceration, especially if there is a chance that the injured eye may regain some function. Additionally, with current advanced surgical techniques, many eyes once considered nonviable now have a fair prognosis.

However, only if the injured eye has completely lost its vision and has no potential for any visual recovery, prevention of SO is done by enucleation of the injured eye preferably within the first 2 weeks of injury. Evisceration—the removal of the contents of the globe while leaving the sclera and extraocular muscles intact—is easier to perform, offers long-term orbital stability, and is more aesthetically pleasing, i.e., a greater measure of movement of the prosthesis and thus a more natural appearance. There is concern, however, that evisceration may lead to a higher incidence of SO compared to enucleation. Several retrospective studies involving over 3000 eviscerations, however, have failed to identify a single case of SO.

Once SO is developed, Immunosuppressive therapy is the mainstay of treatment. When initiated promptly following injury, it is effective in controlling the inflammation and improving the prognosis. Mild cases may be treated with local application of corticosteroids and pupillary dilators. More severe or progressive cases require high-dose systemic corticosteroids for months to years. Patients who become resistant to corticosteroids or develop side effects of long-term corticosteroid therapy (osteoporosis and pathologic fractures, mental status changes, etc.), may be candidates for therapy with chlorambucil, cyclophosphamide, or ciclosporin.

While PEX itself is untreatable as of 2011, it is possible for doctors to minimize the damage to vision and to the optic nerves by the same medical techniques used to prevent glaucoma.

- Eyedrops. This is usually the first treatment method. Eyedrops can help reduce intraocular pressure within the eye. The medications within the eyedrops can include beta blockers (such as levobunolol or timolol) which slow the production of the aqueous humor. And other medications can increase its outflow, such as prostaglandin analogues (e.g. latanoprost). And these medicines can be used in various combinations. In most cases of glaucoma, eyedrops alone will suffice to solve the problem.

- Laser surgery. A further treatment is a type of laser therapy known as trabeculoplasty in which a high-energy laser beam is pointed at the trabecular meshwork to cause it to "remodel and open" and improve the outflows of the aqueous humor. These can be done as an outpatient procedure and take less than twenty minutes. One report suggests this procedure is usually effective.

- Eye surgery. Surgery is the treatment method of last resort if the other methods have not worked. It is usually effective at preventing glaucoma. Eye surgery on PEX patients can be subject to medical complications if the fibers which hold the lens have become weakened because of a buildup from the flakes; if the lens-holding fibers have weakened, then the lens may become loose, and complications from eye surgery may result. In such cases, it is recommended that surgeons act quickly to repair the phacodonesis before the lenses have dropped. A surgeon cuts an opening in the white portion of the eye known as the sclera, and removes a tiny area of the trabecular meshwork which enables the aqueous humor to discharge. This lowers the internal pressure within the eye and lessens the chance of future damage to the optic nerve. Cases with pseudophacodonesis and dislocated IOL have been increasing in number, according to one report. In cataract surgery, complications resulting from PEX include capsular rupture and vitreous loss.

- Drug therapy. There are speculations that if genetics plays a role in PEX, and if the specific genes involved can be identified, that possibly drugs can be developed to counteract these mutations or their effects. But such drugs have not been developed as of 2011.

Patients should continue to have regular eye examinations so that physicians can monitor pressure levels and check whether medicines are working.

Mild conjunctivochalasis can be asymptomatic and in such cases does not require treatment. Lubricating eye drops can be tried but do not often work.

If discomfort persists after standard dry eye treatment and anti-inflammatory therapy, surgery can be undertaken to remove the conjunctival folds and restore a smooth tear film. This conjunctivoplasty surgery to correct conjunctivochalasis typically involves resection of an ellipse-shaped segment of conjunctiva just inferior to the lower lid margin, and is usually followed either by suturing or amniotic membrane graft transplantation to close the wound.

Scleral buckle surgery is an established treatment in which the eye surgeon sews one or more silicone bands (or tyres) to the sclera (the white outer coat of the eyeball). The bands push the wall of the eye inward against the retinal hole, closing the break or reducing fluid flow through it and reducing the effect of vitreous traction thereby allowing the retina to re-attach. Cryotherapy (freezing) is applied around retinal breaks prior to placing the buckle. Often subretinal fluid is drained as part of the buckling procedure. The buckle remains in situ. The most common side effect of a scleral operation is myopic shift. That is, the operated eye will be more short sighted after the operation. Radial scleral buckle is indicated for U-shaped tears or Fishmouth tears, and posterior breaks. Circumferential scleral buckle is indicated for multiple breaks, anterior breaks and wide breaks. Encircling buckles are indicated for breaks covering more than 2 quadrants of retinal area, lattice degeneration located on more than 2 quadrant of retinal area, undetectable breaks, and proliferative vitreous retinopathy.

Argon laser trabeculoplasty (ALT) may be used to treat open-angle glaucoma, but this is a temporary solution, not a cure. A 50-μm argon laser spot is aimed at the trabecular meshwork to stimulate the opening of the mesh to allow more outflow of aqueous fluid. Usually, half of the angle is treated at a time. Traditional laser trabeculoplasty uses a thermal argon laser in an argon laser trabeculoplasty procedure.

A newer type of laser trabeculoplasty uses a "cold" (nonthermal) laser to stimulate drainage in the trabecular meshwork. This newer procedure, selective laser trabeculoplasty (SLT), uses a 532-nm, frequency-doubled, Q-switched , which selectively targets melanin pigment in the trabecular meshwork cells. Studies show SLT is as effective as ALT at lowering eye pressure. In addition, SLT may be repeated three to four times, whereas ALT can usually be repeated only once.

Nd:YAG laser peripheral iridotomy (LPI) may be used in patients susceptible to or affected by angle closure glaucoma or pigment dispersion syndrome. During laser iridotomy, laser energy is used to make a small, full-thickness opening in the iris to equalize the pressure between the front and back of the iris, thus correcting any abnormal bulging of the iris. In people with narrow angles, this can uncover the trabecular meshwork. In some cases of intermittent or short-term angle closure, this may lower the eye pressure. Laser iridotomy reduces the risk of developing an attack of acute angle closure. In most cases, it also reduces the risk of developing chronic angle closure or of adhesions of the iris to the trabecular meshwork.

Diode laser cycloablation lowers IOP by reducing aqueous secretion by destroying secretory ciliary epithelium.

The first line of management for chemical injuries is usually copious irrigation of the eye with an isotonic saline or sterile water. In the cases of chemical burns, one should not try to buffer the solution, but instead it with copious flushing.

Risk factors such as UVB exposure and smoking can be addressed. Although no means of preventing cataracts has been scientifically proven, wearing sunglasses that counteract ultraviolet light may slow their development. While adequate intake of antioxidants (such as vitamins A, C, and E) has been thought to protect against the risk of cataracts, clinical trials have shown no benefit from supplements; though evidence is mixed, but weakly positive, for a potential protective effect of the nutrients lutein and zeaxanthin. Statin use is somewhat associated with a lower risk of nuclear sclerotic cataracts.

Pterygium typically do not require surgery unless it grows to such an extent that it causes visual problems. Some of the symptoms such as irritation can be addressed with artificial tears. Surgery may also be considered for unmanageable symptoms.

Conjunctival auto-grafting is a surgical technique that is an effective and safe procedure for pterygium removal. When the pterygium is removed, the tissue that covers the sclera known as the Tenons layer is also removed. Auto-grafting covers the bare sclera with conjunctival tissue that is surgically removed from an area of healthy conjunctiva. That “self-tissue” is then transplanted to the bare sclera and is fixated using sutures or tissue adhesive.

Uveitis is typically treated with glucocorticoid steroids, either as topical eye drops (prednisolone acetate) or as oral therapy. Prior to the administration of corticosteroids, corneal ulcers must be ruled out. This is typically done using a fluoresence dye test. In addition to corticosteroids, topical cycloplegics, such as atropine or homatropine, may be used. Successful treatment of active uveitis increases T-regulatory cells in the eye, which likely contributes to disease regression.

In some cases an injection of posterior subtenon triamcinolone acetate may also be given to reduce the swelling of the eye.

Antimetabolite medications, such as methotrexate are often used for recalcitrant or more aggressive cases of uveitis. Experimental treatments with Infliximab or other anti-TNF infusions may prove helpful.

The anti-diabetic drug metformin is reported to inhibit the process that causes the inflammation in uveitis.

In the case of herpetic uveitis, anti-viral medications, such as valaciclovir or aciclovir, may be administered to treat the causative viral infection.

Depending on the type of ocular injury, either a "pressure patch" or "shield patch" should be applied. Up until circa 1987, pressure patches were the preferred method of treatment for corneal abrasions in non-contact lens wearers; Multiple controlled studies conducted by accredited organizations such as the American Academy of Ophthalmology have shown that pressure patching is of little or no value in healing corneal abrasions and is actually detrimental to healing in some cases. A Cochrane Review found that patching simple corneal abrasions may not improve healing or reduce pain. Pressure patching should never be used on an individual presenting with a corneal abrasion who has a history of contact lens wear. In this circumstance, a virulent infection caused by the bacterium Pseudomonas aeruginosa is at a clearly delineated increased risk for occurrence. These infections can cause blindness within 24 – 48 hours and there is a possibility that the infection can move into the peri-orbital socket, resulting in the need for evisceration of the eyeball. In rare cases, the infection can enter the brain and cause death to the patient.

In cases of globe penetration, pressure patches should never be applied, and instead a shield patch should be applied that protects the eye without applying any pressure. If a shield patch is applied to one eye, the other eye should also be patched due to eye movement. If the uninjured eye moves, the injured eye will also move involuntarily possibly causing more damage.

Surgeons can remove or peel the membrane through the sclera and improve vision by 2 or more Snellen lines. Usually the vitreous is replaced at the same time with clear (BSS) fluid, in a vitrectomy. Surgery is not usually recommended unless the distortions are severe enough to interfere with daily living, since there are the usual hazards of surgery, infections, and a possibility of retinal detachment. More common complications are high intraocular pressure, bleeding in the eye, and cataracts, which are the most frequent complication of vitrectomy surgery. Many patients will develop a cataract within the first few years after surgery. In fact, the visual distortions and diplopia created by cataracts may sometimes be confused with epiretinal membrane.

Cataract removal can be performed at any stage and no longer requires ripening of the lens. Surgery is usually 'outpatient' and performed using local anesthesia. About 9 of 10 patients can achieve a corrected vision of 20/40 or better after surgery.

Several recent evaluations found that cataract surgery can meet expectations only when significant functional impairment due to cataracts exists before surgery. Visual function estimates such as VF-14 have been found to give more realistic estimates than visual acuity testing alone. In some developed countries, a trend to overuse cataract surgery has been noted, which may lead to disappointing results.

Phacoemulsification is the most widely used cataract surgery in the developed world. This procedure uses ultrasonic energy to emulsify the cataract lens. Phacoemulsification typically comprises six steps:

- Anaesthetic – The eye is numbed with either a subtenon injection around the eye (see: retrobulbar block) or topical anesthetic eye drops. The former also provides paralysis of the eye muscles.

- Corneal incision – Two cuts are made at the margin of the clear cornea to allow insertion of instruments into the eye.

- Capsulorhexis – A needle or small pair of forceps is used to create a circular hole in the capsule in which the lens sits.

- Phacoemulsification – A handheld ultrasonic probe is used to break up and emulsify the lens into liquid using the energy of ultrasound waves. The resulting 'emulsion' is sucked away.

- Irrigation and aspiration – The cortex, which is the soft outer layer of the cataract, is aspirated or sucked away. Fluid removed is continually replaced with a saline solution to prevent collapse of the structure of the anterior chamber (the front part of the eye).

- Lens insertion – A plastic, foldable lens is inserted into the capsular bag that formerly contained the natural lens. Some surgeons also inject an antibiotic into the eye to reduce the risk of infection. The final step is to inject salt water into the corneal wounds to cause the area to swell and seal the incision.

Extracapsular cataract extraction (ECCE) consists of removing the lens manually, but leaving the majority of the capsule intact. The lens is expressed through a 10- to 12-mm incision which is closed with sutures at the end of surgery. ECCE is less frequently performed than phacoemulsification, but can be useful when dealing with very hard cataracts or other situations where emulsification is problematic. Manual small incision cataract surgery (MSICS) has evolved from ECCE. In MSICS, the lens is removed through a self-sealing scleral tunnel wound in the sclera which, ideally, is watertight and does not require suturing. Although "small", the incision is still markedly larger than the portal in phacoemulsion. This surgery is increasingly popular in the developing world where access to phacoemulsification is still limited.

Intracapsular cataract extraction (ICCE) is rarely performed. The lens and surrounding capsule are removed in one piece through a large incision while pressure is applied to the vitreous membrane. The surgery has a high rate of complications.

Cherry eye, if caught early, can be resolved with a downward diagonal-toward-snout closed-eye massage of the affected eye or occasionally self-corrects alone or with antibiotics and steroids. Sometimes the prolapse will correct itself with no interference, or with slight physical manual massage manipulation as often as necessary coupled with medication.

While surgeries do exist to correct for severe cases of floaters, there are currently no medications (including eye drops) that can correct for this vitreous deterioration. Floaters are often caused by the normal aging process and will usually disappear as the brain learns to ignore them. Looking up/down and left/right will cause the floaters to leave the direct field of vision as the vitreous humour swirls around due to the sudden movement. If floaters significantly increase in numbers and/or severely affect vision, then one of the below surgeries may be necessary.

Currently, insufficient evidence is available to compare the safety and efficacy of surgical vitrectomy with laser vitreolysis for the treatment of floaters. A 2017 Cochrane Review did not find any relevant studies that compared the two treatments.

Aggressive marketing campaigns are currently promoting the use of laser vitreolysis for the treatment of floaters. No strong evidence currently exists for the treatment of floaters with laser vitreolysis. Currently, the strongest available evidence comparing these two treatment modalities are retrospective case series.

Enzymatic vitreolysis has been trialled to treat vitreomacular traction (VMT) and anomalous posterior vitreous detachment. Whilst the mechanism of action may have an effect on clinically significant floaters, as of March 2015 there are no clinical trials being undertaken to determine whether this may be a therapeutic alternative to either i) conservative management, or ii) vitrectomy.

Postoperative treatment includes antibiotic eye ointment three times daily for two weeks. With newer procedures, the rate of prolapse recurrence is minimal. Most techniques have a reprolapse rate of approximately zero to four percent. Occasionally, additional or duplicate surgery is required. With treatment, it is possible for animals to live a normal life.

There is no good evidence for any preventive actions, since it appears this is a natural response to aging changes in the vitreous. Posterior vitreous detachment (PVD) has been estimated to occur in over 75 per cent of the population over age 65, that PVD is essentially a harmless condition (although with some disturbing symptoms), and that it does not normally threaten sight. However, since epiretinal membrane appears to be a protective response to PVD, where inflammation, exudative fluid, and scar tissue is formed, it is possible that NSAIDs may reduce the inflammation response. Usually there are flashing light experiences and the emergence of floaters in the eye that herald changes in the vitreous before the epiretinal membrane forms g

The prognosis is generally good for those who receive prompt diagnosis and treatment, but serious complication including cataracts, glaucoma, band keratopathy, macular edema and permanent vision loss may result if left untreated. The type of uveitis, as well as its severity, duration, and responsiveness to treatment or any associated illnesses, all factor into the outlook.

The best treatment for light sensitivity is to address the underlying cause. Once the triggering factor is treated, photophobia disappears in many but not all cases.

People with photophobia will avert their eyes from direct light, such as sunlight and room lights. They may seek the shelter of a dark room. They may wear sunglasses designed to filter peripheral light and wide-brimmed sun hats.

Wearing sunglasses indoors can make symptoms worse over time as it will dark-adapt the retina which aggravates sensitivity to light. Indoor photophobia symptoms may be relieved with the use of precision tinted lenses which block the green-to-blue end of the light spectrum without blurring or impeding vision.

A paper by Stringham and Hammond, published in the "Journal of Food Science", reviews studies of effects of consuming Lutein and Zeaxanthin on visual performance, and notes a decrease in sensitivity to glare.